Rhythmic contractions of a healthy heart are normally controlled by the sinoatrial (SA) node, specialized cells located in the upper right atrium. The SA node is the normal pacemaker of the heart, typically initiating 60–100 heart beats per minute. When the SA node is pacing the heart normally, the heart is said to be in normal sinus rhythm (NSR).
A heart rhythm which deviates from normal sinus rhythm is an arrhythmia. Arrhythmia is a general term used to describe heart rhythm disturbances arising from a variety of physical conditions and disease processes. Bradycardia occurs when the heart rhythm is too slow and has a number of etiological sources including tissue damage due to myocardial infarction, exposure to toxins, electrolyte disorders, infection, drug effects, hypoglycemia or hypothyroidism. Bradycardia also may be caused by the sick sinus syndrome, wherein the SA node loses its ability to generate or transmit an action potential to the atria.
Tachycardia occurs when the rhythm is too fast. The origin of an aberrant tachyarrhythmic impulse may lie in either the atria or the ventricles. Supraventricular tachycardia is an atrial arrhythmia and is often caused by an extra conducting pathway between the atria and ventricles. Such a pathway can allow retrograde conduction or electrical impulses from the ventricles into the atria. The extra pathway in combination with the normal pathway forms a conducting loop that modifies the normal heart rhythm. Atrial flutter is caused due to electrical impulses circulating in the atria. Atrial fibrillation occurs when the pulses occur in the atria at irregular intervals and usually at a rate of greater than 300 impulses per minute. As a result, pulses reaching the AV node and thus the ventricles are also irregular, causing irregular contractions of the ventricles at an increased rate.
Ventricular tachycardia occurs when a pulse is initiated in the ventricular myocardium with a rhythm more rapid than the normal rhythm of the SA node. Ventricular tachycardia (VT), for example, is characterized by a rapid heart beat, 150 to 250 beats per minute and typically results from damage to the ventricular myocardium from a myocardial infarction. Ventricular tachycardia can quickly degenerate into ventricular fibrillation (VF). Ventricular fibrillation is a condition denoted by extremely rapid, nonsynchronous contractions of the ventricles. The rapid and erratic contractions of the ventricles cannot effectively pump blood to the body and the condition is fatal unless the heart is returned to sinus rhythm within a few minutes.
Implantable cardioverter/defibrillators (ICDs) have been used as an effective treatment for patients with serious arrhythmias. ICDs are able to recognize and treat arrhythmias with a variety of tiered therapies. These tiered therapies include providing anti-tachycardia pacing or cardioversion energy for treating ventricular tachycardia and defibrillation energy for treating ventricular fibrillation. To effectively deliver these treatments, the ICD must first identify the type of arrhythmia that is occurring, after which appropriate therapy is provided to the heart. To apply the proper therapy in responding to an episode of arrhythmia, the ICD may compare sensed cardiac signals to a previously stored cardiac waveform. The stored cardiac waveform must accurately characterize a patient's true supraventricular rhythm (SVR) to properly identify potentially fatal deviations.
Various methods have been used to characterize a patient's supraventricular rhythm. Previously described methods often require the acquisition of a relatively large number of heart beat samples to accurately characterize the patient's SVR. These techniques are not suitable for use in all cases. When the heart is being paced, for example, the paced beats are typically discarded from use in template formation. A large number of supraventricular beats may be difficult to acquire for patients requiring intermittent or constant pacing pulses to be applied to the heart. Consequently, for these patients, a characterization of SVR cannot readily be generated or updated by previous methods.
For the reasons stated above, and for other reasons stated below which will become apparent to those skilled in the art upon reading the present specification, there is a need in the art for a method and device that reliably and accurately characterizes a patient's SVR requiring a minimal number of supraventricular beat samples. There exists a further need for such an approach that is adaptive and accommodates changes in the patient's SVR over time. The present invention fulfills these and other needs.